Context Perturbed inositol physiology in insulin resistant conditions has led to proposals of inositol supplementation for gestational diabetes (GDM) prevention, but placental inositol biology is poorly understood. Objective Investigate associations of maternal glycemia with placental inositol content, determine glucose effects on placental expression of inositol enzymes and transporters, and examine relations with birthweight. Design and Participants Case-control study of placentae from term singleton pregnancies (GDM n=24, non-GDM n=26), and culture of another 9 placentae in different concentrations of glucose and myo-inositol for 48h. Main Outcome Measures Placental inositol was quantified by the Megazyme® assay. Relative expression of enzymes involved in myo-inositol metabolism and plasma membrane inositol transport was determined by quantitative RT-PCR and immunoblotting. Linear regression analyses adjusted for maternal age, BMI, ethnicity, gestational age and sex. Results Placental inositol content was 17% lower in GDM compared with non-GDM. Higher maternal mid-gestation glycemia were associated with lower placental inositol. Increasing fasting glycemia was associated with lower protein levels of the myo-inositol synthesis enzyme, IMPA1, and the inositol transporters, SLC5A11 and SLC2A13, the expression of which also correlated with placental inositol content. In vitro, higher glucose concentrations reduced IMPA1 and SLC5A11 mRNA expression. Increasing fasting glycemia positively associated with customized birthweight percentile as expected in cases with low placental inositol, but this association was attenuated with high placental inositol. Conclusion Glycemia-induced dysregulation of placental inositol synthesis and transport may be implicated in reduced placental inositol content in GDM, and this may in turn be permissive to accelerated fetal growth.

The New Zealand glowworm, Arachnocampa luminosa, is well-known for displays of blue-green bioluminescence, but details of its bioluminescent chemistry have been elusive. The glowworm is evolutionarily distant from other bioluminescent creatures studied in detail, including the firefly. We have isolated and characterised the molecular components of the glowworm luciferase-luciferin system using chromatography, mass spectrometry and 1H NMR spectroscopy. The purified luciferase enzyme is in the same protein family as firefly luciferase (31% sequence identity). However, the luciferin substrate of this enzyme is produced from xanthurenic acid and tyrosine, and is entirely different to that of the firefly and known luciferins of other glowing creatures. A candidate luciferin structure is proposed, which needs to be confirmed by chemical synthesis and bioluminescence assays. These findings show that luciferases can evolve independently from the same family of enzymes to produce light using structurally different luciferins.

Short title: Myoinositol alters placental 13 C-labelled fatty acid metabolism 22 Key points summary 23  The placenta regulates the supply of fatty acids and other nutrients from mother to fetus, 24 a process that is disturbed in gestational diabetes. 25  As myo-inositol is being investigated as an intervention to prevent gestational diabetes, 26 we examined the effects of increasing myo-inositol concentrations on the processing of 27 labelled fatty acids in small pieces of human placenta collected immediately after 28 uneventful pregnancies. 29  Myo-inositol's effect on fatty-acid incorporation into placental lipids depended on the 30 type of fatty acid, with palmitic acid, oleic acid and docosahexaenoic acid (saturated, 31 mono-unsaturated and polyunsaturated fatty acids, respectively) showing different 32 changes. 33 All lipids containing the same labelled-fatty-acid showed similar responses to myo-34 inositol, indicating that myo-inositol affects the early stages of fatty-acid processing. 35 The degree of placental responsiveness to myo-inositol in vitro correlated with maternal 36 BMI and glucose levels during pregnancy, suggesting that maternal metabolic 37 characteristics may influence placental responses to myo-inositol. Abstract 41Myo-inositol has been proposed for prevention of gestational diabetes, a condition where 42 placental lipid-processing is disrupted. We investigated in-vitro the effect of myo-inositol on 43 fatty-acid (FA) processing in human term placentas from seven uncomplicated singleton 44 pregnancies, with normal mid-gestation oral glucose tolerance tests. Placental explants were 45 incubated with 13 C-labelled palmitic-acid (PA), 13 C-oleic-acid (OA) and 13 C-docosahexaenoic-46 acid (DHA) (saturated, mono-unsaturated and polyunsaturated respectively) across a range of 47 myo-inositol concentrations for 24h and 48h. The incorporation of labelled-FA into 48 phosphatidylcholines (PC), triacylglycerols (TAG), phosphatidylethanolamines (PE) and 49 lysophosphatidylcholines (LPC) was quantified by liquid-chromatography tandem mass-50 spectrometry. At 24h, myo-inositol addition increased the amounts of 13 C-PA and 13 C-OA 51 labelled lipids relative to controls. Effects (p<0.05, vs control=1) were seen with 30 µM myo-52 inositol (physiological dose) for 13 C-PA-LPC (median fold-change: 1.26, IQR: 1.07-1.38) and 53 13 C-PA-PE (1.17, 1.03-1.62). At 48h, myo-inositol addition increased the amount of 13 C-OA 54 labelled lipids but decreased 13 C-PA and 13 C-DHA labelled lipids. Effects were seen for 13 C-55 OA-PC (1.25, 1.02-1.75), 13 C-OA-PE (1.37, 1.16-1.52) and 13 C-OA-TAG (1.32, 1.21-1.75) 56 with 30 µM myo-inositol and 13 C-DHA-TAG (0.78, 0.72-0.86) with 100 µM myo-inositol. All 57 lipids labelled with the same 13 C-FA showed similar responses to myo-inositol, suggesting that 58 myo-inositol affects upstream processes such as FA uptake or activation. Lipid incorporation 59 and myo-inositol responsivity of 13 C-PA correlated with maternal fasting glycaemia and first 60 trimester BM...

Analysis of lupulin glands gave reliable results for the main quality indicators used by hops breeders, potentially avoiding harvesting, drying and solvent extracting whole hops. PCA of digital X,Y-data rapidly discriminated different hops chemotypes, and highlighted plants with potential for new flavourcultivars. Copyright © 2016 John Wiley & Sons, Ltd.

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We postulate that myo-inositol, a proposed intervention for gestational diabetes, affects transplacental lipid supply to the fetus. We investigated the effect of myo-inositol on fatty acid processing in human placental explants from uncomplicated pregnancies. Explants were incubated with 13C-labeled palmitic acid, 13C-oleic acid and 13C-docosahexaenoic acid across a range of myo-inositol concentrations for 24 h and 48 h. The incorporation of labeled fatty acids into individual lipids was quantified by liquid chromatography mass spectrometry. At 24 h, myo-inositol increased the amount of 13C-palmitic acid and 13C-oleic-acid labeled lipids (median fold change relative to control = 1). Significant effects were seen with 30 µM myo-inositol (physiological) for 13C-palmitic acid-lysophosphatidylcholines (1.26) and 13C-palmitic acid-phosphatidylethanolamines (1.17). At 48 h, myo-inositol addition increased 13C-oleic-acid-lipids but decreased 13C-palmitic acid and 13C-docosahexaenoic-acid lipids. Significant effects were seen with 30 µM myo-inositol for 13C-oleic-acid-phosphatidylcholines (1.25), 13C-oleic-acid-phosphatidylethanolamines (1.37) and 13C-oleic-acid-triacylglycerols (1.32) and with 100 µM myo-inositol for 13C-docosahexaenoic-acid-triacylglycerols (0.78). Lipids labeled with the same 13C-fatty acid showed similar responses when tested at the same time point, suggesting myo-inositol alters upstream processes such as fatty acid uptake or activation. Myo-inositol supplementation may alter placental lipid physiology with unknown clinical consequences.

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Background Fetal docosahexaenoic acid (DHA) supply relies on preferential transplacental transfer, which is regulated by placental DHA lipid metabolism. Maternal hyperglycemia and obesity associate with higher birthweight and fetal DHA insufficiency but the role of placental DHA metabolism is unclear. Methods Explants from 17 term placenta were incubated with 13C-labeled DHA for 48 h, at 5 or 10 mmol/L glucose treatment, and the production of 17 individual newly synthesized 13C-DHA labeled lipids quantified by liquid chromatography mass spectrometry. Results Maternal BMI positively associated with 13C-DHA-labeled diacylglycerols, triacylglycerols, lysophospholipids, phosphatidylcholine and phosphatidylethanolamine plasmalogens, while maternal fasting glycemia positively associated with five 13C-DHA triacylglycerols. In turn, 13C-DHA-labeled phospholipids and triacylglycerols positively associated with birthweight centile. In-vitro glucose treatment increased most 13C-DHA-lipids, but decreased 13C-DHA phosphatidylethanolamine plasmalogens. However, with increasing maternal BMI, the magnitude of the glucose treatment induced increase in 13C-DHA phosphatidylcholine and 13C-DHA lysophospholipids was curtailed, with further decline in 13C-DHA phosphatidylethanolamine plasmalogens. Conversely, with increasing birthweight centile glucose treatment induced increases in 13C-DHA triacylglycerols were exaggerated, while glucose treatment induced decreases in 13C-DHA phosphatidylethanolamine plasmalogens were diminished. Conclusions Maternal BMI and glycemia increased the production of different placental DHA lipids implying impact on different metabolic pathways. Glucose-induced elevation in placental DHA metabolism is moderated with higher maternal BMI. In turn, findings of associations between many DHA lipids with birthweight suggest that BMI and glycemia promote fetal growth partly through changes in placental DHA metabolism.